Multiple environmental stressors, including chemicals termed obesogens, contribute to the susceptibility of organisms to obesity. Bis(2-ethylhexyl)-2,3,4,5-tetrabromophthalate (TBPH), a novel brominated flame retardant, is an environmental contaminant that may disrupt lipid metabolism. However, the risk of TBPH leading to obesity remains unknown. Herein, adult female zebrafish fed a normal-fat diet (NFD) or high-fat diet (HFD) were exposed to 0, 0.02 and 2.0 μM TBPH for 6 weeks. The results showed that chronic TBPH exposure lead to significant weight gain, adipocyte hypertrophy, and subcutaneous fat accumulation, which could be enhanced by HFD feeding. HFD individuals also showed significant visceral fat accumulation. Transcription of the main adipokines regulating lipid metabolism associated with the brain-gut axis were significantly affected by TBPH, especially leptin (brain) and adiponectin (intestine). Additionally, peroxisome proliferator-activated nuclear receptor gamma (PPAR-γ) was significantly upregulated in intestine. TBPH increased the abundance of Firmicutes and Bacteroidetes in the gut microbiota in both NFD and HFD groups, resulting in obesity. Interestingly, population diversity analysis indicated that TBPH alone had a comparable impact on gut microbiota composition to that of HDF controls. Thus, TBPH increased the susceptibility of female zebrafish to obesity by disrupting brain-gut axis regulation and gut microbial composition, leading to enhanced fat accumulation under HFD conditions.

多种环境压力因素，包括称为肥胖的化学物质，有助于生物体对肥胖的易感性。双（2-乙基己基）-2,3,4,5-四溴邻苯二甲酸酯（TBPH）是一种新型溴化阻燃剂，是一种可能破坏脂质代谢的环境污染物。然而，TBPH 导致肥胖的风险仍然未知。在此，喂食正常脂肪饮食 (NFD) 或高脂肪饮食 (HFD) 的成年雌性斑马鱼暴露于 0、0.02 和 2.0 μM TBPH 6 周。结果表明，长期暴露于 TBPH 会导致体重显着增加、脂肪细胞肥大和皮下脂肪堆积，而 HFD 喂养可以增强这种情况。HFD 个体也表现出显着的内脏脂肪堆积。瘦素（大脑）和脂联素（肠）。此外，过氧化物酶体增殖物激活的核受体 γ（PPAR- γ）在肠道中显着上调。TBPH 增加了 NFD 和 HFD 组肠道微生物群中厚壁菌门和拟杆菌门的丰度，导致肥胖。有趣的是，种群多样性分析表明，单独的 TBPH 对肠道微生物群组成的影响与 HDF 对照的影响相当。因此，TBPH 通过破坏脑-肠轴调节和肠道微生物组成增加了雌性斑马鱼对肥胖的易感性，导致在 HFD 条件下脂肪积累增加。